Pain is a prevalent and costly health problem. When pain persists beyond the “natural” course of an illness, extends beyond the typical time required for an injury to heal, or is associated with a progressive illness such as arthritis, the pain is designated chronic. It has been estimated that 86 million Americans suffer with some form of chronic pain (Bonica, 1979). Bonica estimates the cost of chronic pain in the United States at $60 billion annually. Such costs are related to hospitalization, outpatient treatment, medication, surgery, loss of work productivity, loss of income, disability payments, and litigation settlements. The social impact of pain is also considerable.

Recent clinical observations favor the theory that migraine is caused by a primary injury of cerebral neurons with secondary involvement of intracranial and extracranial blood vessels. The primary injury is attributed to disruption of cerebral neurotransmitters and particularly the neuroadrenergic and serotonergic systems. These theories have not explained the importance of environmental factors, which so frequently trigger migraine.

The author suggests that the pineal gland, which is outside the CNS unprotected by blood brain barrier and sensitive to external stimuli, could act as the intermediate causative factor of migraine, via a derangement of melatonin.

Summary

Serotonin released from aggregating platelets can reach sufficient concentrations to affect local vascular function in a number of ways. The monoamine can cause contraction of blood vessels by its direct action on smooth muscle or by potentiating the effect of other vasoconstrictor agents. It can also induce vasodilatation by a direct relaxing effect on smooth muscle, by inhibition of adrenergic nerves, and by release of an uncharacterised relaxing factor from endothelial cells. One of its most likely physiological roles is to aid in haemostasis by promoting platelet aggregation and by causing local vasoconstriction at sites of injury. It probably has a role in some forms of vascular pathology as well: it may contribute to vasospasm of cerebral, coronary, and digital arteries, particularly if there is endothelial dysfunction or damage.

Much evidence has implicated serotonin (5-hydroxytryptamine) in the pathogenesis of migraine. Serotonergic agonists, such as ergotamine, and antagonists, such as methys-ergide and pizotifen, are both used in therapy of migraine. Promising but conflicting early results have not yet defined a place for serotonergic antagonists in other vasospastic disorders. The antihypertensive efficacy of one serotonergic antagonist, ketanserin, raises questions about the possible involvement of serotonin in either the initiation or the maintenance of the elevated peripheral vascular resistance in several forms of hypertension, including essential hypertension.

Subjective stress sensitivity and physiological parameters were compared between 24 migraine subjects and 24 matched headache-free controls during a multifrequency 85-dB (A) aversive auditory Stressor and during a recovery period. Measures consisted of frontalis EMG, temporal artery blood volume pulse, heart rate, a stress sensitivity questionnaire, stress reaction during the stress-expectation period, and ratings of noise aversiveness. Migraine subjects showed a higher level of general stress sensitivity, increased situational stress sensitivity, and higher ratings of noise aversiveness; this supports the general notion that migraine sufferers are psychologically more sensitive toward stress stimulation than nonheadache controls. Physiologically, the migraine subjects differed from the control group only with regard to the temporal blood volume pulse during stress stimulation; this finding is consistent with Wolff's weak-link theory.

Summary

A total of 323 cases of first-ever stroke were registered in the first 2 years of the Oxfordshire Community Stroke Project. Of these patients, 244 (76%) had a stroke due to cerebral infarction. There was a past history of migraine headaches in 56 (17%) of the 323 cases of stroke and in 44 (18%) of the 244 cases of cerebral infarction. A past history of migraine headaches was no commoner in patients with stroke due to cerebral infarction than in those with stroke due to intracranial haemorrhage. One hundred and seventy-three (71%) patients with cerebral infarction had at least one risk factor for ischaemic stroke; the frequency of such risk factors was similar in patients with and without a history of migraine. In 7 (3%) of the 244 patients the cerebral infarction was presumed to be “migrainous”; however, only 3 of these 7 (1.2% of the 24) were free of risk factors for ischaemic stroke. If all 7 cases were considered migrainous, the incidence rate of first migrainous cerebral infarction was 3.36 per 100,000 per year (95% confidence limits 0.87–5.86). If only the 3 patients who were free of risk factors were included, the incidence was 1.44 per 100,000 per year (95% confidence limits 0–3.07).

Serotonin (5-hydroxytryptamine) causes contraction of most large blood vessels and of venules. The vasoconstrictor effects of serotonin can be due to direct activation of the smooth muscle, to amplification of the response to other neurohumoral mediators, or to the liberation of other endogenous vasoconstrictors (e.g. norepinephrine from adrenergic nerves). Vasodilator responses to serotonin are seen mainly at the arteriolar level, but can also be observed in larger blood vessels. They can be due to the release of other endogenous vasodilators (e.g vasoactive intestinal polypeptide from peptidergic nerves), direct relaxation of vascular smooth muscle, inhibition of adrenergic neurotransmission, or production of inhibitory signals by the endothelium. Aggregating platelets release a number of vasoactive materials, including serotonin, and can evoke both vasoconstrictor and vasodilator responses. Hence the absence of endothelial cells or of adrenergic nerve activity may change the primary response to aggregating platelets from dilatation to constriction. Vasconstrictor responses to serotonin released from aggregating platelets may play a role in the etiology of spasm in cerebral, digital and coronary vessels, and in the maintenance of the elevated peripheral resistance in arterial hypertension. A possible involvement of serotonin in the increase in peripheral resistance characteristic of chronic hypertension is suggested by the following observations in hypertensive man or animals: (a) the turnover rate of platelets, the main peripheral source of serotonin, is accelerated; (b) the uptake of serotonin by platelets is reduced; (c) the metabolism of serotonin by the endothelial cells is decreased; (d) the vascular smooth muscles are hyperresponsive to the constrictor effects of serotonin and other serotonergic agonists; (e) the S2 -serotonergic antagonist ketanserin lowers arterial blood pressure in hypertensive humans.

Comparisons were made among patients with IBS (n=55), tension headache (n=69), or migraine headache (n=68) and nonpatient controls (n=64) on the MMPI and several other psychological tests, including BDI, STAI, Life Events, and Psychosomatic Symptom Checklist. With two nonsignificant exceptions (MMPI scale F and Life Events) the groups were consistently ordered, in terms of increasing psychological distress: Normals < Migraine Headache < Tension Headache < IBS. The IBS patients were more like the tension headache patients than any other group. Subgroups of IBS patients, on the basis of presence or absence of diarrhea or constipation in addition to abdominal pain, were generally not significantly different on the psychological tests.

Edmund Jacobson died on January 7, 1983, at the age of 94. A psychologist and physician by training, he made important early contributions to the fields of psychophysiology, psychosomatics, and bio-electronics. He devised one of the most widely used self-control techniques in the overlapping fields of behavior therapy, behavioral medicine, and self-regulation: progressive relaxation. This chapter was stimulated by reflecting on Jacobson’s contributions and evaluating some of his ideas and empirical contributions in light of current concerns and controversies in the various fields in which he worked. In it we shall contrast Jacobson’s original progressive relaxation technique with some of the “revised” progressive relaxation techniques that have been developed over the years. We shall argue that some of these methods are so fundamentally different from Jacobson’s that they require entirely different rationales, and we shall hypothesize that they have very different effects.